INVESTIGATORY PROJECT

Of

CHEMISTRY

Session 2010-11

Hitesh Rana
X11

Common Adulterants/Contaminants
 in food and Simple screening tests
for their detection
Modern-day diets high in hydrogenated vegetable oils instead of
traditional animal fats are implicated in causing a significant increase
in heart disease and cancer.

In 1954 a young researcher from Russia, named David Kritchevsky,

published a paper describing the effects of feeding cholesterol to
rabbits.1 Cholesterol added to vegetarian rabbit chow caused the
formation of atheromas - plaques that block arteries and contribute to
heart disease. Cholesterol is a heavyweight molecule - an alcohol or a
sterol - found only in animal foods such as meat, cheese, eggs and
butter.

In the same year, according to the American Oil Chemists Society,

Kritchevsky published a paper describing the beneficial effects of
polyunsaturated fatty acids for lowering cholesterol levels.2
(Polyunsaturated fatty acids are the kind of fats found in large amounts
in highly liquid vegetable oils made from corn, soybeans, safflower
seeds and sunflower seeds.

Mono-unsaturated fatty acids are found in large amounts in olive oil,

palm oil and lard; saturated fatty acids are found in large amounts in
fats and oils that are solid at room temperature, e.g., butter, tallow and
coconut oil.)

Scientists of the period were grappling with a new threat to public

health: a steep rise in heart disease. While turn-of-the-century
mortality statistics are unreliable, they consistently indicate that heart
disease caused no more than 10 per cent of all deaths - considerably
less than infectious diseases such as pneumonia and tuberculosis. By
1950, coronary heart disease (CHD) was the leading source of
mortality in the United States, causing more than 30 per cent of all
deaths.

The greatest increase came under the rubric of myocardial infarction

(MI) - a massive blood clot leading to obstruction of a coronary artery
and consequent death to the heart muscle. MI was almost non-existent
in 1910 and caused no more than 3,000 deaths per year in 1930. By
1960, there were at least 500,000 MI deaths per year in the US. What
lifestyle changes had caused this increase?
One change was a decrease in infectious disease, following the decline
of the horse as a means of transport, the installation of more sanitary
water supplies and the advent of better housing, all of which allowed
more people to reach adulthood and the heart attack age. The other
was a dietary change.

Since the early part of the century when the US Department of

Agriculture (USDA) had begun to keep track of food 'disappearance'
data (the amount of various foods going into the food supply), a
number of researchers had noticed a change in the kind of fats
Americans were eating.

Butter consumption was declining, while the use of vegetable oils,

especially oils that had been hardened to resemble butter by a process
called 'hydrogenation', was increasing dramatically.

By 1950, butter consumption had dropped from 18 pounds per person

per year to just over 10 pounds. Margarine filled in the gap, rising from
about two pounds per person at the turn of the century to about eight.
Consumption of vegetable shortening - used in crackers and baked
goods - remained relatively steady at about 12 pounds per person per
year, but vegetable oil consumption had more than tripled from just
under three pounds per person per year to more than 10 pounds.3

The statistics pointed to one obvious conclusion: Americans should eat

the traditional foods - including meat, eggs, butter and cheese - that
nourished their ancestors, and avoid the newfangled, vegetable-oil-
based foods that were flooding the grocers' shelves.

The Kritchevsky articles attracted immediate attention because they

lent support to another theory - one that militated against the
consumption of meat and dairy products.

This was the lipid hypothesis: namely, that saturated fat and
cholesterol from animal sources raise cholesterol levels in the blood,
leading to deposition of cholesterol and fatty material as pathogenic
plaques in the arteries.

Kritchevsky's rabbit trials were actually a repeat of studies carried out

four decades earlier in St Petersburg, in which rabbits fed saturated
fats and cholesterol developed fatty deposits in their skin and other
tissues - and in their arteries.

By showing that polyunsaturated oils from vegetable sources lowered

serum cholesterol at least temporarily in humans, Kritchevsky
appeared to show that the findings from the animal trials were relevant
 to the CHD problem, that the lipid hypothesis was a valid explanation
for the new epidemic, and that, by reducing animal products in their
diets, Americans could avoid heart disease.

In the years that followed, a number of population studies

demonstrated that the animal model - especially one derived from
vegetarian animals - was not a valid approach for the problem of heart
disease in human omnivores.

A 1955 report on artery plaques in soldiers killed during the Korean

War showed little difference in the number and severity of plaques
between American soldiers and those of Japanese natives - 75 per cent
versus 65 per cent - even though the Japanese diet at the time was
lower in animal products and fat.4

A 1957 study of the largely vegetarian Bantu found that they had as
much atheroma - occlusions or plaque build-up in the arteries - as
other races from South Africa who ate more meat.5

A 1958 report noted that Jamaican Blacks showed a degree of

atherosclerosis comparable to that found in the United States,
although they suffered from lower rates of heart disease.6

A 1960 report noted that the severity of atherosclerotic lesions in Japan

approached that of the United States.7

The 1968 International Atherosclerosis Project, in which over 22,000

corpses in 14 nations were cut open and examined for plaques in the
arteries, showed the same degree of atheroma in all parts of the world
- in populations that suffered from a great deal of heart disease, and in
populations that had very little or none at all.8

All of these studies pointed to the fact that the thickening of the
arterial walls is a natural, unavoidable process. The lipid hypothesis did
not hold up to these population studies, nor did it explain the tendency
toward fatal clots that caused myocardial infarction.

In 1956, an American Heart Association (AHA) fund-raiser was aired on

all three major networks. The Master of Ceremonies interviewed,
among others, Irving Page and Jeremiah Stamler of the AHA and
researcher Ancel Keys.

Panellists presented the lipid hypothesis as the cause of the heart

disease epidemic and launched the Prudent Diet, one in which corn oil,
margarine, chicken and cold cereal replaced butter, lard, beef and
eggs.
 The television campaign was not an unqualified success because one
of the panellists, Dr Dudley White, disputed his colleagues at the AHA.
Dr White noted that heart disease in the form of myocardial infarction
was non-existent in 1900 when egg consumption was three times what
it was in 1956 and when corn oil was unavailable.

When pressed to support the Prudent Diet, Dr White replied:

"See here, I began my practice as a cardiologist in 1921 and I never

saw an MI patent until 1928. Back in the MI-free days before 1920 the
fats were butter and lard, and I think that we would all benefit from the
kind of diet that we had at a time when no one had ever heard the
word 'corn' oil."

But the lipid hypothesis had already gained enough momentum to

keep it rolling, in spite of Dr White's nationally televised plea for
common sense in matters of diet and in spite of the contradictory
studies that were showing up in the scientific literature.

In 1957, Dr Norman Jolliffe, Director of the Nutrition Bureau of the New

York Health Department, initiated the Anti-Coronary Club in which
selected businessmen, ranging in age from 40 to 59 years, were placed
on the Prudent Diet. Club members used corn oil and margarine
instead of butter, cold breakfast cereals instead of eggs and chicken,
and fish instead of beef.

Anti-Coronary Club members were to be compared with a 'matched'

group of the same age who ate eggs for breakfast and had meat three
times a day. Jolliffe, an overweight diabetic confined to a wheelchair,
was confident that the Prudent Diet would save lives, including his
own.

In the same year, the food industry initiated advertising campaigns

that touted the health benefits of their products: low in fat or made
with vegetable oils. A typical ad read "Wheaties may help you live
longer". Wesson recommended its cooking oil "for your heart's sake".

An ad in the Journal of the American Medical Association (JAMA)

described Wesson oil as a "cholesterol depressant". Mazola
advertisements assured the public that "science finds corn oil
important to your health". Medical journal ads recommended
Fleishmann's unsalted margarine for patients with high blood pressure.

In his syndicated column, Dr Frederick Stare, head of Harvard

University's Nutrition Department, encouraged the consumption of
 corn oil - up to one cup a day. In a promotional piece specifically for
Proctor and Gamble's Puritan oil, he cited two experiments and one
clinical trial as showing that high blood cholesterol is associated with
CHD.

However, both experiments had nothing to do with CHD, and the

clinical trial did not find that reducing blood cholesterol had any effect
on CHD events. Later, Dr William Castelli, director of the Framingham
Study, was one of several specialists to endorse Puritan. Dr Antonio
Gotto, Jr, former AHA president, sent practising physicians a letter
promoting Puritan oil - printed on Baylor College of Medicine, The De
Bakey Heart Center letterhead.9

The irony of Gotto's letter is that De Bakey, the famous heart surgeon,
co-authored a 1964 study involving 1,700 patients, which also showed
no definite correlation between serum cholesterol levels and the
nature and extent of coronary artery disease.10 In other words, those
with low cholesterol levels were just as likely to have blocked arteries
as those with high cholesterol levels.

But while studies like DeBakey's mouldered in the basements of

university libraries, the vegetable oil campaign took on increased
bravado and audacity.

The American Medical Association (AMA) at first opposed the

commercialisation of the lipid hypothesis and warned that "the anti-fat,
anti-cholesterol fad is not just foolish and futile...it also carries some
risk".

The American Heart Association, however, was committed. In 1961,

the AHA published its first dietary guidelines aimed at the public. The
authors, Irving Page, Ancel Keys, Jeremiah Stamler and Frederick Stare,
called for the substitution of polyunsaturates for saturated fat, even
though Keys, Stare and Page had all previously noted in published
papers that the increase in CHD was paralleled by increasing
consumption of vegetable oils. In fact, in a 1956 paper, Keys had
suggested that the increasing use of hydrogenated vegetable oils
might be the underlying cause of the CHD epidemic.11

Stamler showed up again in 1966 as an author of Your Heart Has Nine

Lives, a little self-help book advocating the substitution of vegetable
oils for butter and other so-called 'artery-clogging' saturated fats.

The book was sponsored by makers of Mazola corn oil and Mazola
margarine.
Stamler did not believe that lack of evidence should deter Americans
from changing their eating habits. The evidence, he stated, was
"...compelling enough to call for altering some habits even before the
final proof is nailed down... the definitive proof that middle-aged men
who reduce their blood cholesterol will actually have far fewer heart
attacks waits upon diet studies now in progress."

His version of the Prudent Diet called for substituting low-fat milk
products such as skim milk and low-fat cheeses for cream, butter and
whole cheeses, reducing egg consumption and cutting the fat off red
meats. Heart disease, he lectured, was a disease of rich countries,
striking rich people who ate rich food, including 'hard' fats like butter.

It was in the same year, 1966, that the results of Dr Jolliffe's Anti-
Coronary Club experiment were published in JAMA.12 Those on the
Prudent Diet of corn oil, margarine, fish, chicken and cold cereal had
an average serum cholesterol of 220, compared to 250 in the meat-
and-potatoes control group.

However, the study authors were obliged to note that there were eight
deaths from heart disease among Dr Jolliffe's Prudent Diet group, and
none among those who ate meat three times a day. Dr Jolliffe was
dead by this time. He succumbed in 1961 from a vascular thrombosis,
although the obituaries listed the cause of death as "complications
from diabetes".

The compelling "proof" that Stamler and others were sure would
vindicate wholesale tampering with American eating habits had not yet
been "nailed down".

The problem, said the insiders promoting the lipid hypothesis, was that
the numbers involved in the Anti-Coronary Club experiment were too
small. Dr Irving Page urged a National Diet-Heart Study involving one
million men, in which the results of the Prudent Diet could be
compared on a large scale with those on a diet high in meat and fat.

With great media attention, the National Heart, Lung and Blood
Institute organised the stocking of food warehouses in six major cities,
where men on the Prudent Diet could get tasty polyunsaturated
doughnuts and other fabricated food items free of charge.

But a pilot study, involving 2,000 men, resulted in exactly the same
number of deaths in both the Prudent Diet group and the control
group. A brief report in Circulation (March 1968) stated that the study
was a milestone "in mass environmental experimentation" that would
have "an important effect on the food industry and the attitude of the
 public toward its eating habits".

But the million-man Diet-Heart Study was abandoned in utter silence

"for reasons of cost". Its chairman, Dr Irving Page, died of a heart
attack.

Most animal fats - like butter, lard and tallow - have a large proportion
of saturated fatty acids. Saturated fats are straight chains of carbon
and hydrogen that pack together easily so that they are relatively solid
at room temperature. Oils from seeds are composed mostly of
polyunsaturated fatty acids.

These molecules have kinks in them at the point of the unsaturated

double bond. They do not pack together easily and therefore tend to
be liquid at room temperature.

Judging from both food data and turn-of-the-century cookbooks, the

American diet in 1900 was a rich one, with at least 35 to 40 per cent of
calories coming from fats, mostly dairy fats in the form of butter,
cream, whole milk, and also eggs. Salad dressing recipes usually called
for egg yolks or cream; only occasionally for olive oil. Lard or tallow
served for frying.

Rich dishes like head cheese and scrapple contributed additional

saturated fats during an era when cancer and heart disease were rare.
Butter substitutes made up only a small portion of the American diet,
and these margarines were blended from coconut oil, animal tallow
and lard - all rich in natural saturates.

The technology by which liquid vegetable oils could be hardened to

make margarine was first discovered by a French chemist named
Sabatier. He found that a nickel catalyst would cause the
hydrogenation (the addition of hydrogen to unsaturated bonds to make
them saturated) of ethylene gas to ethane.

Subsequently, the British chemist Norman developed the first

application of hydrogenation to food oils and took out a patent. In
1909, Procter & Gamble acquired the US rights to a British patent on
making liquid vegetable oils solid at room temperature.

The process was used on both cotton-seed oil and lard to give "better
physical properties", to create shortenings that did not melt as easily
on hot days.

The hydrogenation process transforms unsaturated oils into straight

'packable' molecules by rearranging the hydrogen atoms at the double
 bonds. In nature, most double bonds occur in the cis configuration -
that is, with both hydrogen atoms on the same side of the carbon chain
at the point of the double bond. It is the cis isomers of fatty acids that
have a bend or kink at the double bond, preventing them from packing
together easily.

Hydrogenation creates trans double bonds by moving one hydrogen

atom across to the other side of the carbon chain at the point of the
double bond. In effect, the two hydrogen atoms then balance each
other and the fatty acid straightens, creating a packable 'plastic' fat
with a much higher melting temperature.

Although trans fatty acids are technically unsaturated, they are

configured in such a way that the benefits of unsaturation are lost. The
presence of several unpaired electrons presented by contiguous
hydrogen atoms in their cis form allows many vital chemical reactions
to occur at the site of the double bond.

When one hydrogen atom is moved to the other side of the fatty acid
molecule during hydrogenation, the ability of living cells to make
reactions at the site is compromised or altogether lost. Trans fatty
acids are sufficiently similar to natural fats that the body readily
incorporates them into the cell membrane; once there, their altered
chemical structure creates havoc with thousands of necessary
chemical reactions - everything from energy provision to prostaglandin
production.

After the Second World War, 'improvements' made it possible to

plasticise highly unsaturated oils from corn and soybeans. New
catalysts allowed processors to 'selectively hydrogenate' the kinds of
fatty acids found in soy and canola oils - those with three double
bonds.

Called 'partial hydrogenation', this new method allowed processors to

replace cotton-seed oil with more unsaturated corn and soybean oils in
margarines and shortenings. This spurred a meteoric rise in soybean
production from virtually nothing in 1900 to 70 million tons in 1970,
surpassing corn production. Today, soy oil dominates the market and is
used in almost 80 per cent of all hydrogenated oils.

The particular mix of fatty acids in soy oil results in shortenings

containing about 40 per cent trans fats - an increase of about 5 per
cent over cotton-seed oil and 15 per cent over corn oil. Canola oil,
processed from a hybrid form of rape-seed, is particularly rich in fatty
acids containing three double bonds and can contain as much as 50
per cent trans fats.
Trans fats of a particularly problematic type are also formed during the
process of deodorising canola oil, although they are not indicated on
labels for canola oil.

Certain forms of trans fatty acids occur naturally in dairy fats. Trans
vaccenic acid makes up about four per cent of the fatty acids in butter.
It is an interim product which the ruminant animal then converts to
conjugated linoleic acid, a highly beneficial anti-carcinogenic
component of animal fat. Humans seem to utilise the small amounts of
trans vaccenic acid in butter fat without ill effects.

However, most of the trans isomers in modern hydrogenated fats are

new to the human physiology. By the early 1970s, a number of
researchers had expressed concern about their presence in the
American diet, noting that the increasing use of hydrogenated fats had
paralleled the increase in both heart disease and cancer.

The unstated solution was one that could be easily presented to the
public: eat natural, traditional fats; avoid newfangled foods made from
vegetable oils; use butter, not margarine.

But medical research and public consciousness took a different tack -

one that accelerated the decline of traditional foods like meat, eggs
and butter, and fuelled continued dramatic increases in vegetable oil
consumption.

Although the AHA had committed itself to the lipid hypothesis and the
unproven theory that polyunsaturated oils afforded protection against
heart disease, concerns about hydrogenated vegetable oils were
sufficiently great to warrant the inclusion of the following statement in
the organisation's 1968 diet heart statement: "Partial hydrogenation of
polyunsaturated fats results in the formation of trans forms which are
less effective than cis, cis forms in lowering cholesterol concentrations.

It should be noted that many currently available shortenings and

margarines are partially hydrogenated and may contain little
polyunsaturated fat of the natural cis, cis form."

While 150,000 copies of the statement were printed, they were never
distributed. The shortening industry objected strongly, and a
researcher named Fred Mattson of Procter & Gamble convinced
Campbell Moses, medical director of the AHA, to remove it.13 The final
recommendations for the public contained three major points:

restrict calories
 substitute polyunsaturates for saturates
reduce cholesterol in the diet
Other organisations fell in behind the AHA in pushing vegetable oils
instead of animal fats. By the early 1970s, the National Heart, Lung
and Blood Institute, the AMA, the American Dietetic Association and
the National Academy of Sciences had all endorsed the lipid hypothesis
and the avoidance of animal fats for those Americans in the 'at risk'
category.

Since Kritchevsky's early studies, many other trials had shown that
serum cholesterol can be lowered by increasing ingestion of
polyunsaturates. The physiological explanation for this is that when
excess polyunsaturates are built into the cell membranes, resulting in
reduced structural integrity or 'limpness', cholesterol is sequestered
from the blood into the cell membranes to give them 'stiffness'.

The problem was that there was no proof that lowering serum
cholesterol levels could stave off CHD.
Adulteration in food is normally present in its most crude form,
prohibited substances are either added or partly or wholly substituted.
In India normally the contamination/adulteration in food is done either
for financial gain or due to carelessness and lack in proper hygienic
condition of processing, storing, transportation and marketing. This
ultimately results that the consumer is either cheated or often become
victim of diseases. Such types of adulteration are quite common in
developing countries or backward countries. However, adequate
precautions taken by the consumer at the time of purchase of such
produce can make him alert to avoid procurement of such food. It is
equally important for the consumer to know the common adulterants
and their effect on health.

Injurious Adulterants/Contaminants in Foods

and their Health Effects
S.No Adulterant Foods Commonly Diseases or Health
Involved Effects
Adulterants in food
1 Argemone seeds Mustard seeds Epidemic dropsy,
Argemone oil Edible oils and fats Glaucoma,
Cardiac arrest
2 Artificially coloured foreign As a substitute for cumin Injurious to health
seeds seed,
Poppy seed, black pepper
3 Foreign leaves or Tea Injurious to health, cancer
exhausted tea leaves,
saw dust artificially
 coloured
4 TCP Oils Paralysis
5 Rancid oil Oils Destroys vitamin A and E
6 Sand, marble chips, Food grains, pulses etc. Damage digestive tract
stones, filth
7 Lathyrus sativus Khesari dal alone or Lathyrism (crippling spastic
Mixed in other pulses paraplegia)
Chemical
Contaminatio
n
8 Mineral oil (white oil, Edible oils and fats, Cancer
petroleum fractions) Black pepper
9 Lead chromate Turmeric whole and Anemia, abortion, paralysis,
powdered, mixed spices brain damage
10 Methanol Alcoholic liquors Blurred vision, blindness,
death
11 Arsenic Fruits such as apples Dizziness, chills, cramps,
sprayed over with lead paralysis, death
arsenate
12 Barium Foods contaminated by rat Violent peristalisis, arterial
poisons (Barium carbonate) hypertension, muscular
twitching, convulsions,
cardiac disturbances
13 Cadmium Fruit juices, soft drinks, etc. ‘Itai-itai (ouch-ouch) disease,
in contact with cadmium Increased salivation, acute
plated vessels or gastritis, liver and kidney
equipment. Cadmium damage, prostrate cancer
contaminated water and
shell-fish
14 Cobalt Water, liquors Cardiac insufficiency and
mycocardial failure
15 Lead Water, natural and Lead poisoning (foot-drop,
processed food insomnia, anemia,
constipation, mental
retardation, brain damage)

16 Copper Food Vomiting, diarrhoea

17 Tin Food Colic, vomiting
18 Zinc Food Colic, vomiting
19 Mercury Mercury fungicide treated Brain damage, paralysis,
seed grains or mercury death
contaminated fish

NOTE : Safe limits have been prescribed for above metals in different food.
Continuous use of food contaminated with these metals beyond safe limits
may cause these diseases
Bacterial
contamination
20 Bacillus cereus Cereal products, custards, Food infection (nausea,
puddings, sauces vomiting, abdominal pain,
diarrhoea)
21 Salmonella spp. Meat and meat products, Salmonellosis (food infection
 raw vegetables, salads, usually with fever and chills)
shell-fish, eggs and egg
products, warmed-up
leftovers
22 Shigella sonnei Milk, potato, beans, poultry, Shigellosis (bacillary
tuna, shrimp, moist mixed dysentery)
foods
23 Staphylococcus aureus Dairy products, baked foods Increased salivation,
Entero-toxins-A,B,C,D or especially custard or cream- vomiting, abdominal cramp,
E filled foods, meat and meat diarrhoea, severe thirst, cold
products, low-acid frozen sweats, prostration
foods, salads, cream
sauces, etc.
24 Clostridium botulinus Defectively canned low or Botulism (double vision,
toxins medium-acid foods; meats, muscular paralysis, death
A,B,E or F sausages, smoked vacuum- due to respiratory failure)
packed fish, fermented food
etc.
25 Clostridium.perfringens Milk improperly processed Nausea, abdominal pains,
(Welchii) type A or canned meats, fish and diarrhoea, gas formation
gravy stocks
26 Diethyl stilbestrol (additive Meat Sterlites, fibroid tumors etc.
in animal feed)
27 3,4 Benzopyrene Skoked food Cancer
28 Excessive solvent residue Solvent extracted oil, oil Carcinogenic effect
cake etc.
29 Non-food grade or Food Blood clot, angiosarcoma,
contaminated cancer etc.
packing material
30 Non-permitted colour or Coloured food Mental retardation, cancer
permitted food colour and other toxic effect.
beyond safe limit
31 BHA and BHT beyond Oils and fats Allergy, liver damage,
safe limit increase in serum
chloresterol etc.
32 Monosodium Chinese food, meat and Brain damage, mental
glutamate(flour) meat products retardation in infants
(beyond safe limit)
33 Coumarin and dihydro Flavoured food Blood anticoagulant
coumarin
34 Food flavours beyond Flavoured food Chances of liver cancer
safe limit
35 Brominated vegetable oils Cold drinks Anemia, enlargement of
heart
36 Sulphur dioxide and In variety of food as Acute irritation of the gastro-
sulphite beyond safe preservative intestinal tracts etc.
limit
37 Artificial sweetners Sweet foods Chances of cancer
beyond safe limit
Fungal contamination
38 Aflatoxins Aspergillus flavus- Liver damage and cancer
contaminated foods such as
groundnuts, cottonseed, etc.
39 Ergot alkaloids from Ergot-infested bajra, rye Ergotism (St.Anthony’s fire-
Claviceps purpurea meal or bread burning sensation in
 Toxic alkaloids, extremities, itching of skin,
ergotamine, peripheral gangrene)
ergotoxin and
ergometrine groups
40 Toxins from Grains (millet, wheat, oats, Alimentary toxic
Fusarium sporotrichioides rye,etc) aleukia(ATA) (epidemic
panmyelotoxicosis)
41 Toxins from Fusarium Moist grains Urov disease (Kaschin-Beck
sporotrichiella disease)
42 Toxins from Yellow rice Toxic mouldy rice disease
Penicillium inslandicum
Penicillium atricum,
Penicillium citreovirede,
Fusarium, Rhizopus,
Aspergillus
43 Sterigmatocystin from Foodgrains Hepatitis
Aspergillus versicolour
Aspergillus nidulans and
bipolaris
44 Ascaris lumbricoides Any raw food or water Ascariasis
contaminated by human
faces containing eggs of the
parasite
45 Entamoeba histolytica Raw vegetables and fruits Amoebic dysentery
Viral

46 Virus of infectious Shell-fish, milk, unheated Infectious hepatitis

Hepatitis (virus A) foods contaminated with
faeces, urine and blood of
infected human
47 Machupo virus Foods contaminated with Bolivian haemorrhagic fever
rodents urine, such as
cereals
Natural
Contamination
48 Flouride Drinking water, sea foods, Excess fluoride causes
tea, etc. fluorosis (mottling of teeth,
skeletal and neurological
disorders)
49 Oxalic acid Spinach, amaranth, etc. Renal calculi, cramps, failure
of blood to clot
50 Gossypol Cottonseed flour and cake Cancer
51 Cyanogenetic compounds Bitter almonds, apple seeds, Gastro-intestinal
cassava, some beans etc. disturbances
52 Polycyclic Aromatic Smoked fish, meat, mineral Cancer
Hydrocarbons(PAH) oil-contaminated water, oils,
fats and fish, especially
shell-fish
53 Phalloidine (Alkaloid) Toxic mushrooms Mushroom poisoning
(Hypoglycemia, convulsions,
profuse watery stools,
severe necrosis of liver
leading to hepatic failure and
death)
54 Solanine Potatoes Solanine poisoning
 (vomiting, abdominal pain,
diarrhoea)
55 Nitrates and Nitrites Drinking water, spinach Methaemoglobinaemia
rhubarb, asparagus, etc. especially in infants, cancer
and meat products and tumours in the liver,
kidney, trachea oesophagus
and lungs. The liver is the
initial site but afterwards
tumours appear in other
organs.
56 Asbestos (may be present Polished rice, pulses, Absorption in particulate
in talc, Kaolin, etc. processed foods containing form by the body may
and in processed anti-caking agents, etc. produce cancer
foods)
57 Pesticide residues All types of food Acute or chronic poisoning
(beyond safe limit) with damage to nerves and
vital organs like liver, kidney,
etc.
58 Antibiotics (beyond safe Meats from antibiotic-fed Multiple drug resistance
limit) animals hardening of arteries, heart
disease